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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Phosphorylation-regulated endoplasmic reticulum retention signal in the renal outer-medullary K+ channel (ROMK)
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Phosphorylation-regulated endoplasmic reticulum retention signal in the renal outer-medullary K+ channel (ROMK)

机译：磷酸化调节肾内髓质K +通道（ROMK）中的内质网保留信号

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摘要

The renal outer-medullary K+ channel (ROMK; Kir1.1) mediates K+ secretion in the renal mammalian nephron that is critical to both sodium and potassium homeostasis. The posttranscriptional expression of ROMK in the plasma membrane of cells is regulated by delivery of protein from endoplasmic reticulum (ER) to the cell surface and by retrieval by dynamin-dependent endocytic mechanisms in clathrin-coated pits. The S44 in the NH12 terminus of ROMK1 can be phosphorylated by PKA and serum- and glucocorticoid-inducible kinase-1, and this process increases surface expression of functional channels. We present evidence that phosphorylation of S44 modulates channel expression by increasing its cell surface delivery consequent to suppression of a COOH-terminal ER retention signal. This phosphorylation switch of the ER retention signal could provide a pool of mature and properly folded channels for rapid delivery to the plasma membrane. The x-ray crystal structures of inward rectifier K+ channels have shown a close apposition of the NH2 terminus with the distal COOH terminus of the adjacent subunit in the channel homotetramer, which is important to channel gating. Thus, NH2-terminal phosphorylation modifying a COOH-terminal ER retention signal in ROMK1 could serve as a checkpoint for proper subunit folding critical to channel gating.
机译：肾髓外K +通道（ROMK; Kir1.1）介导肾哺乳动物肾单位中的K +分泌，这对钠和钾稳态均至关重要。 ROMK在细胞质膜中的转录后表达受蛋白质从内质网（ER）传递到细胞表面的调节，并通过在网格蛋白包被的凹坑中通过依赖动力的内吞机制进行恢复。 ROMK1的NH12末端的S44可以被PKA以及血清和糖皮质激素诱导的激酶1磷酸化，该过程增加了功能通道的表面表达。我们目前的证据表明，S44的磷酸化通过增加其细胞表面传递从而抑制COOH末端ER保留信号来调节通道表达。 ER保留信号的这种磷酸化开关可以提供一组成熟且适当折叠的通道，以快速递送至质膜。内向整流器K +通道的X射线晶体结构显示NH2末端与通道同四聚体中相邻亚基的远端COOH末端紧密并列，这对通道门控很重要。因此，修改ROM​​K1中COOH末端ER保留信号的NH 2末端磷酸化可作为检查通道门控关键亚基折叠的检查点。

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